Does stenting for atherosclerotic renovascular disease improve blood pressure and kidney function better than medical treatment?

612 Atherosclerotic renovascular disease (ARD) is a common condition in which the atheroscle‐ rotic narrowing of renal arteries may lead to renin‐dependent hypertension, progressive re‐ nal dysfunction, and/or recurrent pulmonary edema.1 It typically occurs in high‐risk patients with coexistent vascular disease elsewhere.2 Con‐ sequently, most patients with ARD are likely to die from coronary heart disease or stroke before end‐stage renal failure occurs. The incidence of re‐ nal artery thrombosis is less than 1% per year.3,4 The risk of chronic renal replacement therapy is 18 times lower than that of a major cardiovascu‐ lar event.5‐7 Stenting aims at reducing blood pressure (BP), stabilizing or improving renal function, and pre‐ venting cardiovascular and renal events in pa‐ tients with ARD. Controlled trials comparing medication plus stenting to medication alone, medication plus surgery, or medication plus an‐ gioplasty without stenting provided disappoint‐ ing results (TABLE).8‐11 Most patients undergoing stenting to treat hypertension associated with ARD, still require antihypertensive agents after the procedure because the reduction in BP follow‐ ing stenting is modest, and because several anti‐ hypertensive agents, such as renin‐angiotensin antagonists or β‐blockers, are needed to prevent cardiovascular and renal events even in patients with normalized BP. Two recent trials compared renal outcome in ARD patients provided with medication plus stenting with that in ARD pa‐ tients supplied with medication alone.11,12 Their results have shown that stenting does not pre‐ serve renal function. Improvements in revascu‐ larization techniques did not alter BP or renal outcomes of angioplasty. Compared with angio‐ plasty alone, angioplasty plus stenting improved renal artery patency but did not improve BP con‐ trol or renal function.8 Compared with stenting alone, stenting plus protection devices and intra‐ venous platelet inhibition did not improve renal function.9 The main explanation for these neg‐ ative results is that ARD involves downstream renal parenchymal lesions that cannot be im‐ proved by revascularization.13 A trial comparing the effects of medication alone (including an an‐ giotensin II receptor antagonist) and medication plus renal artery stenting on cardiovascular out‐ comes is currently underway.14 Stenting for ARD does not improve BP and kidney function better than medical treatment. Besides, it is associated with frequent compli‐ cations. Thirty‐one of the 226 stented patients (13.7%) in the trials summarized in the TABLE suf‐ fered major complications as defined by current criteria.15 Stable patients with ARD should be treated first with medical management.16 Avail‐ able trials did not include unstable patients with uncontrollable hypertension or with pulmonary edema. It is therefore possible, yet unproved, that renal artery stenting is useful in patients with ARD and refractory hypertension or heart fail‐ ure, or that it is preferable to abstention in ARD patients given a renin‐angiotensin antagonist. With or without revascularization, medical ther‐ apy using hypolipidemic and antiplatelet agents and renin‐angiotensin antagonists7 is required for the prevention of renal and cardiovascular events in patients with ARD. EDITORIAL